Biological Trace Element Research最新文献

The aim of this study was to explore the role of the ZnT9 protein in obesity-induced sperm maturation disorders in men. We generated a mouse model of obesity-induced weak spermatogenesis via a high-fat diet (HFD) for 10 weeks. In addition to the HFD, a 5-week intervention of salubrinal (SAL) (an inhibitor of endoplasmic reticulum stress) (1 mg/kg/day), ZnSO₄ (15 mg/kg/day), and their combination was started at week 6, after which sperm viability and epididymal tissue damage were assessed. To investigate the role of the ZnT9 protein in spermatogenesis, the expression levels of the ZnT9 protein, endoplasmic reticulum stress (ERS)-related protein, Wnt pathway protein, and apoptosis-related protein in epididymal tissue were measured. Compared with those in the normal (N) group, the mice in the HFD group presented decreased sperm motility, damaged epididymal tissue, epididymal tissue showed decreased expression of ZnT9, β-catenin, LEF protein and mRNA, and increased expression of total cholesterol (TC) and triglycerides (TG), GRP78, Caspase-3, BAX protein and mRNA, as well as increased apoptosis as shown by TUNEL staining. Compared with the HFD group, HFD + ZnSO₄ group, HFD + SAL group, and HFD + ZnSO₄ + SAL groups resulted in reduced epididymal damage, improved decreased total cholesterol (TC) and triglycerides (TG), sperm viability, increased expression of ZnT9, β-catenin, LEF protein and mRNA, and decreased expression of GRP78, Caspase-3, and BAX protein and mRNA, as well as decreased apoptosis as shown by TUNEL staining in epididymal tissues. According to this study, obesity leads to elevated ERS and affects ZnT9 protein synthesis. Inhibition of the Wnt pathway ultimately leads to cell death and damage in epididymal tissue and decreased sperm viability.

As teeth develop, their mineralised composition is a bio-recorder of diet, environment, and growth. High-resolution elemental mapping provides a tool to reveal records of life history within teeth. The relative concentrations of a range of trace elements change between in utero development, birth, and weaning in eutherian mammals. Marsupials, however, have a different mode of development: altricial birth and growth within the pouch facilitated by compositional transitions in milk. How these differences alter patterns of elemental mineralisation and become recorded in marsupial teeth is previously unknown. This study analyses the distribution of calcium (major element), zinc (actively incorporated trace element), and strontium (passively incorporated trace element) in the teeth of five species of diprotodontian marsupial using synchrotron X-ray fluorescence microscopy. We find that the diprotodontian lower incisor concatenates elemental variation from across the molariform dentition, preserving a prolonged record of life history in four of the five species. Patterns of elemental incorporation in enamel, dentine, and cementum are presented, with Ca, Zn, and Sr having differing distributions. Zn accretion indicates a role in mineralisation and/or prevention of tooth degradation. Zn also demarcates incremental cementum lines. Sr is shown to be passively incorporated into marsupial teeth, with increasing Sr concentration in milk recorded in dental tissues formed contemporaneously. Older individuals have oscillatory signals in Sr that appear linked to seasonality. These findings highlight some similarities between eutherian and marsupial trace element incorporation, particularly in the distribution of Zn. Sr signals in marsupial teeth record key aspects of life history.

Iron overload has been shown to have deleterious effects in the brain through the formation of reactive oxygen species, which ultimately may contribute to neurodegenerative disorders. Accordingly, rodent studies have indicated that systemic administration of iron produces excess iron in the brain and results in behavioral and cognitive deficits. To what extent cognitive abilities are affected and which neurobiological mechanisms underlie those deficits remain to be more fully characterized. In the present study, we looked at the effects of a 30 mg/kg iron sub-chronic treatment on cognitive abilities in two hippocampal-dependent spatial tasks (place navigation, spatial/non-spatial object recognition), in relation with iron content and oxidative stress biomarkers (MDA, SOD, CAT) in the cerebellum, hippocampus, prefrontal cortex and striatum, four brain areas known to be involved in the processing of spatial information. Iron-treated rats were impaired in acquisition and retention of the platform location in the navigation task and in the spatial/non-spatial object recognition task. Iron content and MDA were found to be increased in the four brain regions of interest, but activity of the antioxidant enzymes was not modified. The results indicate that the ability of rats to process spatial information whether in place navigation or spontaneous object spatial/non-spatial recognition is disrupted following a 30 mg/kg sub-chronic treatment. The deficits are hypothesized to result from iron excess-induced oxidative stress in the network of brain areas involved in the processing of spatial information.

Several studies have reported associations between specific heavy metals and essential trace elements and acute myocardial infarction (AMI). However, there is limited understanding of the relationships between trace elements and AMI in real-life co-exposure scenarios, where multiple elements may interact simultaneously. This cross-sectional study measured serum levels of 56 trace elements using inductively coupled plasma mass spectrometry. We identified individual trace elements linked to AMI using four feature selection methods and evaluated their associations with AMI prevalence and severity through multiple-element logistic regression. Restricted cubic spline analysis was employed to examine non-linear associations. Additionally, we explored the associations between trace element mixtures and AMI prevalence and severity using Bayesian kernel machine regression (BKMR) and element risk score (ERS). Finally, we investigated the potential mechanisms linking trace element exposure to AMI. We detected stable positive associations and linear relationships between Cu and Rb and AMI prevalence and severity. Furthermore, lower Fe concentrations were associated with higher AMI prevalence, while higher Sb concentrations were linked to greater AMI severity. Both BKMR and ERS models indicated positive associations between trace element mixtures and AMI prevalence and severity. Mediation analysis suggested that high-sensitivity C-reactive protein partially mediated the associations between trace elements and AMI prevalence and severity. We provide the first epidemiological evidence of the associations between serum trace element mixtures and AMI prevalence and severity. Under conditions of trace element co-exposure, Cu, Rb, Fe, and Sb were closely associated with AMI. Additionally, our results indicate that hsCRP (inflammation) may be a potential mechanism linking trace elements to AMI.

Selenium (Se) intake or selenoprotein overexpression can cause abnormal glucose metabolism and increase the risk of type 2 diabetes (T2D). The purpose of this study is to observe whether glycolysis bypass in the de novo serine synthesis pathway (SSP) is activated under high-Se stress in vitro. Initially, HCT-116, L02, HepG2, and differentiated C2C12 cells were exposed to five selenomethionine (SeMet) concentrations (0.001 to 10 µmol/L) for 48 h. The expressions of glutathione peroxidase 1 (GPX1), selenoprotein P (SELENOP), 3-phosphoglycerate dehydrogenase (PHGDH), and serine hydroxy-methyltransferases 1 (SHMT1) were assessed by western blotting (WB). Then, corresponding to the peak expressions of GPX1, SELENOP, and PHGDH, 0.1 µmol/L SeMet was identified as the highest intervention concentration. With more detailed levels of SeMet (0.001 to 0.1 µmol/L) given, the differentiated C2C12 cells were treated for 48 h to analyze the expressions of selenoproteins, enzymes related with serine metabolism and insulin signaling pathway. Among the four cell lines, the expressions of selenoproteins and metabolic enzymes of serine in C2C12 cells were more sensitive to changes in Se concentrations, which was similar to that in L02 cells. In C2C12 cells, the expressions of GPX1, SELENOP, selenoprotein N (SELENON), PHGDH, and SHMT1 exhibited a parabolic inflection point at SeMet concentrations of 0.05 µmol/L or 0.075 µmol/L, while 5,10-methylenetetrahydrofolate reductase (MTHFR) and methionine synthase (MS) showed no such trend. After 15 min of insulin stimulation, glucose retained more in the culture medium due to the decreased uptake by C2C12 cells. The expressions of key enzymes (AKT, AKT (Ser-473), AKT (Thr-308), mTOR, and PI3K) in the PI3K-AKT-mTOR signaling pathway decreased with the increased level of SeMet. This study demonstrated that excessive Se intake could induce abnormal glucose metabolism via SSP and impair the normal signaling of insulin in the differentiated C2C12 cells.

Premature ovarian insufficiency (POI) is poorly understood, with causes identified in only 25% of cases. Emerging evidence suggests links between trace elements (TEs) and POI. This study is the first to compare concentrations of manganese (Mn), copper (Cu), zinc (Zn), selenium (Se), molybdenum (Mo), arsenic (As), cadmium (Cd), mercury (Hg), and lead (Pb) across urine, serum, and whole blood in women with POI compared to healthy controls (HC), aiming to explore their distribution and potential associations with POI. This cross-sectional-case-control study enrolled 81 participants (40 POI patients and 41 healthy controls) at the University Medical Centre Ljubljana, Slovenia. Blood and urine samples were collected to quantify basic biochemical parameters using standard clinical chemistry methods and concentrations of Mn, Cu, Zn, Se, Mo, As, Cd, Hg, and Pb using inductively coupled plasma-mass spectrometry (ICP-MS). Participants also completed questionnaires on socio-demographics, medical history, lifestyle, and nutrition. Data was analyzed using the Mann-Whitney U test, Student's t-tests, Fisher exact test, logistic regression models adjusted on body mass index (BMI), age, hematocrit, and Kendall's tau correlation. Women with POI had significantly higher BMI and red blood cell (RBC) indices, including hemoglobin, hematocrit, and red cell distribution width (RDW), compared to controls. A larger proportion of POI patients resided in rural agricultural areas. Liver and kidney function assessments showed no significant differences between the groups. Adjusted models revealed that POI patients had significantly lower urinary levels of Cu, Zn, Se, Mo, Cd, Hg, and Pb than controls, while whole blood Mn levels were higher. Serum Cu levels were significantly elevated in POI patients, whereas Pb, Cd, and Hg were lower. No significant differences were observed for As. Correlation analysis showed several strong to moderate associations among TEs across biofluids, but only weak correlations were found between TEs and demographic or biochemical factors. This study suggests potential associations between TEs and POI in women. Notably, most TEs (Zn, Se, Cu, Mo, Cd, Hg, Pb) were significantly lower in the urine of the POI group, while Cu, Cd, Hg, and Pb showed significant differences in both urine and serum.

Arsenic in drinking water has been associated with an increased risk of health concerns. This metalloid is ingested and distributed throughout the body, accumulating in several organs, including the testis. In this organ, arsenic disturbs steroidogenesis and spermatogenesis and affects male fertility. Although testicular impairment induced by arsenic is well documented, it is still controversial whether such disturbance remains days after the removal of arsenic insult. Therefore, we used a meta-analytical approach to evaluate the magnitude of arsenic effects on testicular parameters and verify whether a withdrawal period can mitigate these alterations. The search terms 'testis" and 'arsenic' were used in PubMed/Medline, Scopus, and Web of Science databases. A total of 1,217 articles were obtained from the literature search, and 73 articles were included in this meta-analysis. Our results showed that arsenic negatively affected hormone synthesis and secretion, testicular weight, tubular and intertubular morphometry, and daily sperm production 24 h after ending exposure. Arsenic inhibited antioxidant enzyme activity, culminating in high oxidative metabolite production and apoptosis occurrence. Most of these effects were not observed in the testis between eight and fifty days after arsenic withdrawal, remaining endocrine dysregulation and oxidative metabolite production. Sodium arsenite was the most toxic compound to the testis at subchronic exposure. These findings shed light on the plasticity and regenerative capacity of testicular interstitium and spermatogonial stem cell niche. However, sexual hormone imbalance remained after arsenic removal. This review evidenced the importance of understanding its toxicity's short- and long-term effects on male reproductive competence.

Prostate cancer (PC) is a common malignancy among men globally. Although genetic, hormonal, and environmental factors contribute to its development, the role of heavy metals remains unclear. This study evaluated serum levels of arsenic, cadmium, lead, mercury, and nickel in PC patients compared to healthy controls. An extensive search of PubMed, Embase, Scopus, and Google Scholar identified relevant studies published up to December 2023. Studies reporting the mean and standard deviation of serum heavy metal levels in PC patients and controls were included. Random-effects models were used to estimate mean differences (MD) or standardized mean differences (SMD) with 95% confidence intervals (CIs). Heterogeneity was evaluated based on I² index, and publication bias was examined using funnel plots. Seven studies involving 691 participants were included. No significant difference was found in serum levels of arsenic between PC patients and controls (MD: 0.04, 95% CI: [-0.15, 0.23]; p = 0.68). Cadmium (SMD: 0.93, 95% CI: [-0.06, 1.93]; p = 0.07) and lead (SMD: 0.65, 95% CI: [-0.22, 1.52]; p = 0.14) were higher in PC patients but not statistically significant. Mercury levels also showed no substantial difference (MD: 0.22, 95% CI: [-0.27, 0.70]; p = 0.38). However, serum nickel levels were significantly higher in PC patients (SMD: 0.62, 95% CI: [0.07, 1.16]; p = 0.03). The study demonstrated a substantial increase in serum concentration of nickel in PC patients compared to controls, indicating a potential role of nickel in PC pathogenesis. Although other heavy metals showed elevated levels in PC patients, these differences were not statistically significant. Further research is needed to explore nickel as a potential biomarker for early PC detection.

The study aimed to examine the interaction between diets supplemented with zinc-L-selenomethionine (ZnSeMet) and two stocking densities (SD) on Nile tilapia (Oreochromis niloticus) males. Four extruded diets were formulated: 0.0, 0.5, 1.0, and 2.0 mg ZnSeMet kg^-1. Fish (58.00 g) were reared at a low SD (LSD) (15 fish tank^-1 or 4,35 kg m^-3) and a high SD (HSD) (45 fish tank^-1 or 13,05 kg m^-3). They were randomly distributed in eight treatments in triplicate in a recirculatory aquaculture system (200 L) and were fed until apparent satiation thrice daily for 65 days. The interaction between LSD and 1.0 or 2.0 mg ZnSeMet kg^-1 was better than other treatments for final weight (116.50-174.83 vs. 97.33-139.17 g), weight gain (108.83.50-116.83 vs. 39.00-80.83 g), relative weight gain (188.03-201.18 vs. 66.25-139.40%), total final length (20.12-20.63 vs. 17.33-19.00 cm), specific growth rate (1.76-1.83 vs. 0.85-1.45% day^-1) (p < 0.05). In general, the interaction between LSD and 1.0 mg ZnSeMet kg^-1 compared to several treatments, showed an increase in plasma total protein (3.23 vs. 2.67-2.78 g dL^-1) and total cholesterol (93.67 vs. 68.50-76.67 mg dL^-1) levels and a reduction in aspartate aminotransferase activity (14.83 vs. 145.67-155.17 U L^-1) (p < 0.05). The highest values for albumin (0.83 vs. 0.57 g dL^-1), glucose (56.00 vs. 45.09 mg dL^-1), and triglycerides (122.33 vs. 68.87 mg dL^-1) in the plasma, erythrocytes (2.22 vs. 2.13 × 10⁶ µL^-1), hemoglobin (9.82 vs. 9.26 g dL^-1), and hematocrit (33.09 vs. 30.21%) were observed in LSD than HSD-reared fish (p < 0.05). In conclusion, adding 1.0 mg ZnSeMet kg^-1 at LSD improved fish growth and hemato-biochemical parameters, but it was not effective at HSD.

Cadmium is a heavy metal contaminant known to cause various health issues. However, limited research exists on the serum metabolomic effects of cadmium exposure in children. In this study, we recruited 42 children to analyze their serum metabolomic profiles, along with measuring urinary cadmium and creatinine concentrations, to evaluate the impact of environmental cadmium exposure on serum metabolism. We also screened for potential biomarkers. The findings revealed that environmental cadmium exposure led to disruptions in amino acid metabolism, biosynthesis of secondary metabolites, endocrine function, lipid metabolism, nervous system function, sensory processes, and the metabolism of cofactors and vitamins in children. Lansioside C, Hydroxytanshinone, and 1-Methylinosine were identified as potential biomarkers. In conclusion, environmental cadmium exposure negatively impacts children's neurological development by inducing metabolic disturbances and increasing the risk of oxidative stress-related disorders. This study provides a valuable theoretical foundation for future efforts to prevent the harmful effects of cadmium exposure in children and mitigate associated health risks.